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INFECTIVE ENDOCARDITIS

Understand the complexities of infective endocarditis: from microbial invasion to cardiac tissue destruction. Learn about etiology, pathogenesis, symptoms, and complications of this serious condition.

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INFECTIVE ENDOCARDITIS

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  1. INFECTIVE ENDOCARDITIS

  2. INFECTIVE ENDOCARDITIS Colonisation / invasion of HEART VALVES & ENDOCARDIUM by a microbe Bulky friable vegetations Destruction of cardiac tissues

  3. Reddish vegetations in the aortic valve in acute endocarditis

  4. “Classification” “Acute” Affects normal heart valves Rapidly destructive Commonly Staph, beta-strep If not treated, usually fatal within 6 weeks “Subacute” Often affects damaged heart valves Indolent nature Strep viridans - better prognosis

  5. Etiology & Pathogenesis • Organisms • Events leading to seeding of blood • Abnormal Heart • Host factors

  6. Organisms S. Viridans Most common causative organism Gram negative bacilli Neonates & immunocompromised Prosthetic valves HACEK organisms Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella Frequently affect damaged valves and can cause emboli

  7. Events Seeding of Blood • Obvious infection elsewhere • Dental / surgical proceedure bacteriemia • Injection of contaminated material by Drug abusers • Occult sources in gut / oral cavity

  8. Abnormal Heart • RHD (Rheumatic Heart Disease) • Myxomatous degeneration of Mitral valve • Degenerative calcific valvular stenosis • Bicuspid aortic valves • Prosthetic valves

  9. Host Factors • Neutropenia • Immunodeficiency • Malignancy • Diabetis Mellitus • Alcohol & drug abuse

  10. Pathogenesis • Thrombi • Hemodynamic • Microbe adherence

  11. Pathogenesis Turbulent blood flow disrupts the endocardium making it “sticky” Bacteremia delivers the organisms to the endocardial surface Adherence of the organisms to the endocardial surface Eventual invasion of the valvular leaflets

  12. Prosthetic Heart Valve a serious complication positive blood culture in patients with underlying prosthetic valves can be a harbinger of endocarditis 12

  13. IV Drug Use Recurrent Polymicrobial Staph aureus tricuspid valve 13

  14. Pathology Local destruction of intracardiac infection: valve, chordae tendineae, fistula, paravalvular abscess, conduction Distant embolization with infarct or infection: 45—65% (autopsy), 70% pulmonary embolism

  15. Pathology • Hematogenous seeding with bacteremia: metastatic infection, • Immune-complex or antibody reaction: IgM, IgA, IgG, Rheumatoid factor, Osler’s node, Roth’s spot

  16. Morphology • Friable bulky vegetations on Heart valves containing fibrin , inflammatory cells, bacteria • Aortic & Mitral valves most affected • Right side valves – drug abusers • Ring abscess • Septic infarcts in brain , kidneys , myocardium , other tissues

  17. Acute Bacterial endocarditis in Aortic Valve

  18. Mitral valve , left atrial posterior wall , IE jet lesion

  19. Microscopy - Vegetations

  20. Layer of fibrin & platelets • Bacterial colonies • Inflammatory reaction on the cusp

  21. Vegetation in active infective endocarditis- fibrin , neutrophils , monocytes

  22. Microvegetation on top of a broad based healing vegetation

  23. CARDIAC VEGETATIONS • Rheumatic heart disease • IE • NBTE • Libman-Sacks endocarditis (SLE)

  24. Nonbacterial thrombotic endocarditis (NBTE)Marantic Malignancy, DIC, uremia, burns, valvular heart disease, intracardiac catheter

  25. NBTE • Small masses of fibrin & platelets • No organisms

  26. NBTE

  27. NBTE

  28. VALVE CUSP

  29. Libman – Sacks Endocarditis • Seen in SLE • Mitral & Tricuspid valvulitis • Small , sterile vegetations on the valvular endocardium , undersurface , chords , mural endocardium of atria & ventricles • Histologically – • - finely granular fibrinous eosinophillic material with haematoxylin bodies • -Valvulitis

  30. LIBMAN SACKS ENDOCARDITIS

  31. Symptoms Acute High grade fever and chills Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V onset of symptoms - usually ~2 weeks or less from the initiating bacteremia

  32. Clubbing

  33. petechiae

  34. Subconjunctival Hemorrhages

  35. Splinter Hemorrhages • Nonblanching • Linear reddish-brown lesions found under the nail bed • Usually do NOT extend the entire length of the nail

  36. Splinter Hemorrhage

  37. Janeway lesions are small erythematous or hemorrhagic, macular, nontender lesions on the palms and soles and are the consequence of septic embolic events.

  38. Janeway Lesions

  39. Janeway Lesions

  40. Osler nodes are small, tender subcutaneous nodules that develop in the pulp of the digits or occasionally more proximally in the fingers and persist for hours to several days.

  41. Osler’s Nodes

  42. Osler’s Nodes

  43. Roth spots are oval retinal hemorrhages with pale centers.

  44. Roth’s Spots

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